多次活性炭灌胃对大鼠血浆敌敌畏浓度的影响

Objective To assess the therapeutic effects of activated charcoal on the acute dichlorvos poisoning in rats. Method Thirty male clean grade Wistar rats were randomly (random number) divided into three groups: control group (group A, n = 10), single dose activated charcoal group (group B, n = 10) and multi-dose activated charcoal (group C, n=10). The rats of group A were suffered from 35 mg/kg dichlorvos exposure by oral without activated charcoal and senna. The rats of group B received 35 mg/kg dichlorvos exposure by oral with 175 mg/kg activated charcoal given immediately after dichlorvos exposure and 35 mg/kg senna given half an hour later. In the group C, 35 mg/kg dichlorvos was given to rats by oral with 175 mg/kg activated charcoal given immediately after dichlorvos exposure and 35 mg/kg senna given half an hour later and then every four hours. Blood samples were collected from the carotid artery at different intervals after exposure. DDVP concentration and total blood acetyl-cholinesterase activity were detected. Differences in serum DDVP concentration, Cmax, AUC (0→∞ ), MRT and acetylcholinesterase among three groups were calculated by using ANOVA. Results Serum DDVP levels in single dose group and in multi-dose group were significantly different from those in control group (P < 0.05). The DDVP levels in multi-dose group were significantly different from those in single dose group 4 hours after exposure (P < 0.05). The AUC and Cmax in activated charcoal treatment groups were significantly different from those in control group (P < 0.05). There were no significant differences in MRT among three groups. Fours hours after exposure to dichlorvos,the levels of serum acetylcholinesterase in rats of group B and group C were significantly different from that in rats of group A (P < 0.05), and there was no significant difference in acetylcholinesteras between group B and group C (P > 0.05). Another four hours later, no differences in acetylcholinesterase were found a-mong three groups (P > 0.05). Conclusions The peak concentrations of dichlorvos in blood are lower in group B and group C, and the blood acetylcholinesterase inhibition is quelled by activated charcoal. Therefore, the effects of multi - dose of activated charcoal is better than that of single dose of activated charcoal.     

多次活性炭灌胃对大鼠血浆敌敌畏浓度的影响

Objective To assess the therapeutic effects of activated charcoal on the acute dichlorvos poisoning in rats. Method Thirty male clean grade Wistar rats were randomly (random number) divided into three groups: control group (group A, n = 10), single dose activated charcoal group (group B, n = 10) and multi-dose activated charcoal (group C, n=10). The rats of group A were suffered from 35 mg/kg dichlorvos exposure by oral without activated charcoal and senna. The rats of group B received 35 mg/kg dichlorvos exposure by oral with 175 mg/kg activated charcoal given immediately after dichlorvos exposure and 35 mg/kg senna given half an hour later. In the group C, 35 mg/kg dichlorvos was given to rats by oral with 175 mg/kg activated charcoal given immediately after dichlorvos exposure and 35 mg/kg senna given half an hour later and then every four hours. Blood samples were collected from the carotid artery at different intervals after exposure. DDVP concentration and total blood acetyl-cholinesterase activity were detected. Differences in serum DDVP concentration, Cmax, AUC (0→∞ ), MRT and acetylcholinesterase among three groups were calculated by using ANOVA. Results Serum DDVP levels in single dose group and in multi-dose group were significantly different from those in control group (P < 0.05). The DDVP levels in multi-dose group were significantly different from those in single dose group 4 hours after exposure (P < 0.05). The AUC and Cmax in activated charcoal treatment groups were significantly different from those in control group (P < 0.05). There were no significant differences in MRT among three groups. Fours hours after exposure to dichlorvos,the levels of serum acetylcholinesterase in rats of group B and group C were significantly different from that in rats of group A (P < 0.05), and there was no significant difference in acetylcholinesteras between group B and group C (P > 0.05). Another four hours later, no differences in acetylcholinesterase were found a-mong three groups (P > 0.05). Conclusions The peak concentrations of dichlorvos in blood are lower in group B and group C, and the blood acetylcholinesterase inhibition is quelled by activated charcoal. Therefore, the effects of multi - dose of activated charcoal is better than that of single dose of activated charcoal.     

氨基胍与左旋硝基精氨酸甲酯在兔心脏骤停复苏中的比较

Objective To observe the changes of nitric oxide (NO) levels in plasma during cardiopul-monary resuscitation (CPR) and to compare the effects of aminoguanidine (AG) and NG-nitro-L-arginine methyl ester (L-NAME) on CPR. Method This was a prospective, randomized animal study performed at the Function Laboratory of Lanzhou University. Cardiac arrest was electrically induced and was left untreated for 5 min. After performing chest compression for 1 min, 40 domestic rabbits were divided into four groups (n = 10) to receive ei-ther 20 mg/kg AG, 25 mg/kg L-NAME, 0.02 mg/kg epinephrine or 2 ml saline placebo before defibrillation. Successfully resuscitated rabbits were observed for a further 4 h. Hernodynamics variables and cardiac functions were monitored with appropriate instrumentation. Arterial blood NO levels were examined at baseline, at the end of 1 min chest compression and at 15, 30, 60 and 120 min after survival. Repeated measures analysis of variance was used to determine statistical significance between groups. Results During chest compression, the mean + stan-dard deviation coronary perfusion pressure was higher in the AG group (40±10 mmHg) than in the L-NAME group (34±8 mmHg; P =0.001) and was higher in both groups with the control group (20±5 mmHg; both P =0.000). Left ventricular + dp/dtmax and- dp/dtmax were higher in the AG group than in the L-NAME group. In the surviving rabbits, the left ventricular + dp/dtmax and - dp/dtmax were higher in the AG and L-NAME groups than in the epinephrine and control groups and were higher in the AG group (4783±912, 4409±827 mmHg/s)than in the b-NAME group (3554±847, 3398±764 mmHg/s; P = 0.001 and 0.023, respectively). Conclu-sions Both AG and L-NAME increased the coronary perfusion pressure, and improved left ventricular systolic and diastolic function during CPR and prevented post-resuscitation myocardial dysfunction. However, AG was signifi-canfly superior to L-NAME.     

氨基胍与左旋硝基精氨酸甲酯在兔心脏骤停复苏中的比较

Objective To observe the changes of nitric oxide (NO) levels in plasma during cardiopul-monary resuscitation (CPR) and to compare the effects of aminoguanidine (AG) and NG-nitro-L-arginine methyl ester (L-NAME) on CPR. Method This was a prospective, randomized animal study performed at the Function Laboratory of Lanzhou University. Cardiac arrest was electrically induced and was left untreated for 5 min. After performing chest compression for 1 min, 40 domestic rabbits were divided into four groups (n = 10) to receive ei-ther 20 mg/kg AG, 25 mg/kg L-NAME, 0.02 mg/kg epinephrine or 2 ml saline placebo before defibrillation. Successfully resuscitated rabbits were observed for a further 4 h. Hernodynamics variables and cardiac functions were monitored with appropriate instrumentation. Arterial blood NO levels were examined at baseline, at the end of 1 min chest compression and at 15, 30, 60 and 120 min after survival. Repeated measures analysis of variance was used to determine statistical significance between groups. Results During chest compression, the mean + stan-dard deviation coronary perfusion pressure was higher in the AG group (40±10 mmHg) than in the L-NAME group (34±8 mmHg; P =0.001) and was higher in both groups with the control group (20±5 mmHg; both P =0.000). Left ventricular + dp/dtmax and- dp/dtmax were higher in the AG group than in the L-NAME group. In the surviving rabbits, the left ventricular + dp/dtmax and - dp/dtmax were higher in the AG and L-NAME groups than in the epinephrine and control groups and were higher in the AG group (4783±912, 4409±827 mmHg/s)than in the b-NAME group (3554±847, 3398±764 mmHg/s; P = 0.001 and 0.023, respectively). Conclu-sions Both AG and L-NAME increased the coronary perfusion pressure, and improved left ventricular systolic and diastolic function during CPR and prevented post-resuscitation myocardial dysfunction. However, AG was signifi-canfly superior to L-NAME.     

氨基胍与左旋硝基精氨酸甲酯在兔心脏骤停复苏中的比较

Objective To observe the changes of nitric oxide (NO) levels in plasma during cardiopul-monary resuscitation (CPR) and to compare the effects of aminoguanidine (AG) and NG-nitro-L-arginine methyl ester (L-NAME) on CPR. Method This was a prospective, randomized animal study performed at the Function Laboratory of Lanzhou University. Cardiac arrest was electrically induced and was left untreated for 5 min. After performing chest compression for 1 min, 40 domestic rabbits were divided into four groups (n = 10) to receive ei-ther 20 mg/kg AG, 25 mg/kg L-NAME, 0.02 mg/kg epinephrine or 2 ml saline placebo before defibrillation. Successfully resuscitated rabbits were observed for a further 4 h. Hernodynamics variables and cardiac functions were monitored with appropriate instrumentation. Arterial blood NO levels were examined at baseline, at the end of 1 min chest compression and at 15, 30, 60 and 120 min after survival. Repeated measures analysis of variance was used to determine statistical significance between groups. Results During chest compression, the mean + stan-dard deviation coronary perfusion pressure was higher in the AG group (40±10 mmHg) than in the L-NAME group (34±8 mmHg; P =0.001) and was higher in both groups with the control group (20±5 mmHg; both P =0.000). Left ventricular + dp/dtmax and- dp/dtmax were higher in the AG group than in the L-NAME group. In the surviving rabbits, the left ventricular + dp/dtmax and - dp/dtmax were higher in the AG and L-NAME groups than in the epinephrine and control groups and were higher in the AG group (4783±912, 4409±827 mmHg/s)than in the b-NAME group (3554±847, 3398±764 mmHg/s; P = 0.001 and 0.023, respectively). Conclu-sions Both AG and L-NAME increased the coronary perfusion pressure, and improved left ventricular systolic and diastolic function during CPR and prevented post-resuscitation myocardial dysfunction. However, AG was signifi-canfly superior to L-NAME.     

氨基胍与左旋硝基精氨酸甲酯在兔心脏骤停复苏中的比较

Objective To observe the changes of nitric oxide (NO) levels in plasma during cardiopul-monary resuscitation (CPR) and to compare the effects of aminoguanidine (AG) and NG-nitro-L-arginine methyl ester (L-NAME) on CPR. Method This was a prospective, randomized animal study performed at the Function Laboratory of Lanzhou University. Cardiac arrest was electrically induced and was left untreated for 5 min. After performing chest compression for 1 min, 40 domestic rabbits were divided into four groups (n = 10) to receive ei-ther 20 mg/kg AG, 25 mg/kg L-NAME, 0.02 mg/kg epinephrine or 2 ml saline placebo before defibrillation. Successfully resuscitated rabbits were observed for a further 4 h. Hernodynamics variables and cardiac functions were monitored with appropriate instrumentation. Arterial blood NO levels were examined at baseline, at the end of 1 min chest compression and at 15, 30, 60 and 120 min after survival. Repeated measures analysis of variance was used to determine statistical significance between groups. Results During chest compression, the mean + stan-dard deviation coronary perfusion pressure was higher in the AG group (40±10 mmHg) than in the L-NAME group (34±8 mmHg; P =0.001) and was higher in both groups with the control group (20±5 mmHg; both P =0.000). Left ventricular + dp/dtmax and- dp/dtmax were higher in the AG group than in the L-NAME group. In the surviving rabbits, the left ventricular + dp/dtmax and - dp/dtmax were higher in the AG and L-NAME groups than in the epinephrine and control groups and were higher in the AG group (4783±912, 4409±827 mmHg/s)than in the b-NAME group (3554±847, 3398±764 mmHg/s; P = 0.001 and 0.023, respectively). Conclu-sions Both AG and L-NAME increased the coronary perfusion pressure, and improved left ventricular systolic and diastolic function during CPR and prevented post-resuscitation myocardial dysfunction. However, AG was signifi-canfly superior to L-NAME.     

氨基胍与左旋硝基精氨酸甲酯在兔心脏骤停复苏中的比较

Objective To observe the changes of nitric oxide (NO) levels in plasma during cardiopul-monary resuscitation (CPR) and to compare the effects of aminoguanidine (AG) and NG-nitro-L-arginine methyl ester (L-NAME) on CPR. Method This was a prospective, randomized animal study performed at the Function Laboratory of Lanzhou University. Cardiac arrest was electrically induced and was left untreated for 5 min. After performing chest compression for 1 min, 40 domestic rabbits were divided into four groups (n = 10) to receive ei-ther 20 mg/kg AG, 25 mg/kg L-NAME, 0.02 mg/kg epinephrine or 2 ml saline placebo before defibrillation. Successfully resuscitated rabbits were observed for a further 4 h. Hernodynamics variables and cardiac functions were monitored with appropriate instrumentation. Arterial blood NO levels were examined at baseline, at the end of 1 min chest compression and at 15, 30, 60 and 120 min after survival. Repeated measures analysis of variance was used to determine statistical significance between groups. Results During chest compression, the mean + stan-dard deviation coronary perfusion pressure was higher in the AG group (40±10 mmHg) than in the L-NAME group (34±8 mmHg; P =0.001) and was higher in both groups with the control group (20±5 mmHg; both P =0.000). Left ventricular + dp/dtmax and- dp/dtmax were higher in the AG group than in the L-NAME group. In the surviving rabbits, the left ventricular + dp/dtmax and - dp/dtmax were higher in the AG and L-NAME groups than in the epinephrine and control groups and were higher in the AG group (4783±912, 4409±827 mmHg/s)than in the b-NAME group (3554±847, 3398±764 mmHg/s; P = 0.001 and 0.023, respectively). Conclu-sions Both AG and L-NAME increased the coronary perfusion pressure, and improved left ventricular systolic and diastolic function during CPR and prevented post-resuscitation myocardial dysfunction. However, AG was signifi-canfly superior to L-NAME.     

氨基胍与左旋硝基精氨酸甲酯在兔心脏骤停复苏中的比较

Objective To observe the changes of nitric oxide (NO) levels in plasma during cardiopul-monary resuscitation (CPR) and to compare the effects of aminoguanidine (AG) and NG-nitro-L-arginine methyl ester (L-NAME) on CPR. Method This was a prospective, randomized animal study performed at the Function Laboratory of Lanzhou University. Cardiac arrest was electrically induced and was left untreated for 5 min. After performing chest compression for 1 min, 40 domestic rabbits were divided into four groups (n = 10) to receive ei-ther 20 mg/kg AG, 25 mg/kg L-NAME, 0.02 mg/kg epinephrine or 2 ml saline placebo before defibrillation. Successfully resuscitated rabbits were observed for a further 4 h. Hernodynamics variables and cardiac functions were monitored with appropriate instrumentation. Arterial blood NO levels were examined at baseline, at the end of 1 min chest compression and at 15, 30, 60 and 120 min after survival. Repeated measures analysis of variance was used to determine statistical significance between groups. Results During chest compression, the mean + stan-dard deviation coronary perfusion pressure was higher in the AG group (40±10 mmHg) than in the L-NAME group (34±8 mmHg; P =0.001) and was higher in both groups with the control group (20±5 mmHg; both P =0.000). Left ventricular + dp/dtmax and- dp/dtmax were higher in the AG group than in the L-NAME group. In the surviving rabbits, the left ventricular + dp/dtmax and - dp/dtmax were higher in the AG and L-NAME groups than in the epinephrine and control groups and were higher in the AG group (4783±912, 4409±827 mmHg/s)than in the b-NAME group (3554±847, 3398±764 mmHg/s; P = 0.001 and 0.023, respectively). Conclu-sions Both AG and L-NAME increased the coronary perfusion pressure, and improved left ventricular systolic and diastolic function during CPR and prevented post-resuscitation myocardial dysfunction. However, AG was signifi-canfly superior to L-NAME.     

氨基胍与左旋硝基精氨酸甲酯在兔心脏骤停复苏中的比较

Objective To observe the changes of nitric oxide (NO) levels in plasma during cardiopul-monary resuscitation (CPR) and to compare the effects of aminoguanidine (AG) and NG-nitro-L-arginine methyl ester (L-NAME) on CPR. Method This was a prospective, randomized animal study performed at the Function Laboratory of Lanzhou University. Cardiac arrest was electrically induced and was left untreated for 5 min. After performing chest compression for 1 min, 40 domestic rabbits were divided into four groups (n = 10) to receive ei-ther 20 mg/kg AG, 25 mg/kg L-NAME, 0.02 mg/kg epinephrine or 2 ml saline placebo before defibrillation. Successfully resuscitated rabbits were observed for a further 4 h. Hernodynamics variables and cardiac functions were monitored with appropriate instrumentation. Arterial blood NO levels were examined at baseline, at the end of 1 min chest compression and at 15, 30, 60 and 120 min after survival. Repeated measures analysis of variance was used to determine statistical significance between groups. Results During chest compression, the mean + stan-dard deviation coronary perfusion pressure was higher in the AG group (40±10 mmHg) than in the L-NAME group (34±8 mmHg; P =0.001) and was higher in both groups with the control group (20±5 mmHg; both P =0.000). Left ventricular + dp/dtmax and- dp/dtmax were higher in the AG group than in the L-NAME group. In the surviving rabbits, the left ventricular + dp/dtmax and - dp/dtmax were higher in the AG and L-NAME groups than in the epinephrine and control groups and were higher in the AG group (4783±912, 4409±827 mmHg/s)than in the b-NAME group (3554±847, 3398±764 mmHg/s; P = 0.001 and 0.023, respectively). Conclu-sions Both AG and L-NAME increased the coronary perfusion pressure, and improved left ventricular systolic and diastolic function during CPR and prevented post-resuscitation myocardial dysfunction. However, AG was signifi-canfly superior to L-NAME.     

氨基胍与左旋硝基精氨酸甲酯在兔心脏骤停复苏中的比较

Objective To observe the changes of nitric oxide (NO) levels in plasma during cardiopul-monary resuscitation (CPR) and to compare the effects of aminoguanidine (AG) and NG-nitro-L-arginine methyl ester (L-NAME) on CPR. Method This was a prospective, randomized animal study performed at the Function Laboratory of Lanzhou University. Cardiac arrest was electrically induced and was left untreated for 5 min. After performing chest compression for 1 min, 40 domestic rabbits were divided into four groups (n = 10) to receive ei-ther 20 mg/kg AG, 25 mg/kg L-NAME, 0.02 mg/kg epinephrine or 2 ml saline placebo before defibrillation. Successfully resuscitated rabbits were observed for a further 4 h. Hernodynamics variables and cardiac functions were monitored with appropriate instrumentation. Arterial blood NO levels were examined at baseline, at the end of 1 min chest compression and at 15, 30, 60 and 120 min after survival. Repeated measures analysis of variance was used to determine statistical significance between groups. Results During chest compression, the mean + stan-dard deviation coronary perfusion pressure was higher in the AG group (40±10 mmHg) than in the L-NAME group (34±8 mmHg; P =0.001) and was higher in both groups with the control group (20±5 mmHg; both P =0.000). Left ventricular + dp/dtmax and- dp/dtmax were higher in the AG group than in the L-NAME group. In the surviving rabbits, the left ventricular + dp/dtmax and - dp/dtmax were higher in the AG and L-NAME groups than in the epinephrine and control groups and were higher in the AG group (4783±912, 4409±827 mmHg/s)than in the b-NAME group (3554±847, 3398±764 mmHg/s; P = 0.001 and 0.023, respectively). Conclu-sions Both AG and L-NAME increased the coronary perfusion pressure, and improved left ventricular systolic and diastolic function during CPR and prevented post-resuscitation myocardial dysfunction. However, AG was signifi-canfly superior to L-NAME.     

氨甲酰化促红细胞生成素逆转慢性心力衰竭大鼠左室重构的研究

目的:探讨氨甲酰化促红细胞生成素(CEPO)对慢性心力衰竭(CHF)大鼠左心室重构的影响。方法:健康雄性Wistar大鼠90只,随机选取10只作为对照组,其余腹腔注射异丙肾上腺素(ISO)进行造模。5周后将造模成功者再分为CHF组和CEPO组,后者腹腔注射CEPO50μg/kg,2次/周,CHF组和对照组同期腹腔注射等量生理盐水,4周后检测各组大鼠血流动力学指标、血浆B型脑钠肽(BNP)水平,并计算左心室重量指数(LVW/BW)。结果:与对照组相比,CHF组左室内压峰值(LVSP)、左室内压上升/下降最大速率(±dp/dtmax)显著降低,左室舒张末压(LVEDP)显著升高(P<0.05),血浆BNP水平显著升高(P<0.05),LVW/BW也显著升高(P<0.05)。与CHF组相比,CEPO组LVSP、±dp/dtmax均显著升高,而LVEDP则显著降低(P<0.05),血浆BNP水平显著降低(P<0.01),LVW/BW也显著降低(P<0.05)。结论:CEPO可通过降低血浆BNP水平、减轻左心室重构来改善CHF大鼠的心功能。     

胚胎干细胞梗死区中心和周边移植治疗急性心肌梗死

背景:现有治疗手段不足以补充梗死心肌,研究表明干细胞移植有可能促使心肌和血管再生,改善心功能和预后.目的:观察急性心肌梗死区中心和周边移植胚胎干细胞后心肌组织形态学及血液动力学的变化.设计、时间及地点:随机对照动物观察,于2007-03/2008-10在中南大学湘雅医学院人体解剖学与神经生物学系神经生物学实验室完成.材料:SPF级Wistar大鼠40只,随机分为4组:正常对照组、梗死模型组、中心移植组、周边移植组,10只/组.胚胎干细胞-D3株(embryonic stem cells-D3,ES-D3)、布法罗大鼠肝细胞均由中国科学院上海细胞所提供.方法:ES-D3细胞复苏后,以(2.0～5.0)× 107L-1种植于培养瓶中,加入含布法罗大鼠肝细胞的条件培养基体外培养分化.除正常对照组外,余3组结扎冠状动脉左前降支建立急性心肌梗死模型.造模后1周接受细胞移植,ES-D3细胞于移植前1 d进行BrdU标记,以胚胎干细胞培养基调整密度至1×109L-1.中心移植组在梗死区选3个点,每点注入10 μL细胞悬液(含104个细胞)至心室壁内;周边移植组在梗死区周边选3个点同法注入等量细胞悬液.主要观察指标:免疫组化及血流动力学指标检测结果.结果:布法罗大鼠肝细胞条件培养基体外培养的ES-D3细胞,呈相对规则的巢状集落样生长,分化8d即可见部分拟胚体出现自发的节律性收缩活动,心肌肌钙蛋白T免疫染色呈阳性,电镜下可见肌管、肌纤维等肌性结构,证实已分化为心肌细胞.周边移植组BrdU免疫荧光染色呈阳性,而中心移植组呈阴性,进一步对BrdU免疫荧光染色阳性细胞行双抗染色,可见心肌肌钙蛋白T呈阳性表达.移植后4周与正常对照组比较,梗死模型组左室收缩、dp/dtmax均减小(P＜0.01),左室舒张末期压上升(P＜0.01),左室质量、左室质量指数均升高(P＜0.01).与梗死模型组比较,中心移植组各项血流动力学指标无明显变化(P＞0.05);周边移植组左室收缩压、±dp/dtmax均显著升高(P＜0.01),左室舒张末期压显著减小(P＜0.01),左室质量、左室质量指数,梗死面积均显著减小(P＜0.01).结论:急性心肌梗死后于梗死周边区移植胚胎干细胞可以阻止心室重构、减少瘢痕面积、改善心功能.     

高敏心肌肌钙蛋白T水平与维持性血液透析患者心脏结构和功能的关系

目的 研究高敏心肌肌钙蛋白（hs-cTnT）与维持性血液透析（maintenance hemodialysis,MHD）患者心脏结构和功能的关系.方法 选择86例规律血液透析的慢性肾衰竭患者（每周3次,时间＞6月）,病情稳定,已排除近6个月内曾发生急性心肌梗死、急性心肌炎事件及肥厚性心肌病者,测定血清hs-cTnT、B型脑钠肽（BNP）、生化指标,同时应用心脏超声心动图测量左室射血分数（LVEF）、左室舒张末内径（LVDd）、室间隔厚度（IVST）、左心室后壁厚度（LVPWT）,计算左室心肌重量指数（LVMI）,分析hs-cTnT与心脏结构和功能指标间的关系.同时检测同期来院体检的60名健康体检者的hs-cTnT作对比分析.结果 维持性血液透析组hs-cTnT水平与健康对照组比较明显升高[（0.263±0.038） ng/ml比（0.016±0.008） ng/ml],差异有统计学意义（P＜0.05）,患者中hs-cTnT与BNP、LVMI及LVH呈正相关（P＜0.05）,与LVEF呈负相关（P =0.015）.结论 hs-cTnT的检测对维持性血液透析患者的早期心脏左室肥厚及收缩功能减退有预测作用.     

急性有机磷农药中毒患者血清肌钙蛋白T与心肌酶学的变化及意义

目的:探讨急性有机磷农药中毒(AOPP)患者肌钙蛋白及心肌酶学变化规律与中毒程度的关系。方法:对92例AOPP患者抽取中毒后1、2、3、5、7天空腹静脉血两组各3mL,对患者的肌钙蛋白T及心肌酶学(CK-MB、CK、AST、LDH)进行测定并将结果与30例健康体检者(抽血一次,两组各3mL)作为对照组进行比较。结果:AOPP患者肌钙蛋白T与心肌酶学均有不同程度的增高,与中毒程度相一致,并随病情好转而恢复。结论:AOPP患者肌钙蛋白T及心肌酶学水平变化能够作为较好地判断中毒程度及预后的参考指标之一。     

心肺复苏后猪各主要脏器组织和超微结构的变化及对血流动力学的影响

目的 通过建立心搏骤停室颤-心肺复苏模型,观察心肺复苏后猪心肌、大脑、肺脏、肝脏及肾脏组织普通病理和超微结构的变化及对血流动力学的影响.方法 16头北京长白猪(29～35kg)随机(随机数字法)分为正常组(n=8)与复苏组(n=8).前组动物仅进行麻醉及气管插管,不予致室颤及心肺复苏.后组动物在建立心搏骤停室颤模型4 min后给予标准心肺复苏术,恢复自主循环(ROSC)10 min后以0.5 mL/(h·kg)的速度持续静脉泵入生理盐水直至复苏后6 h,并分别于致颤前,ROSC后0.5 h,2 h,4 h,6 h监测心排血量(CO)、左心室收缩期压力最大上升速率(+dp/dtmax)、左心室舒张期最大下降速率(-dp/dtmax)、心率(HR)、平均动脉压(MAP),两组动物均于复苏6 h后静脉麻醉下处死,速取其左心室心尖、大脑顶叶皮层、左肺、肝右叶、右肾上极组织行普通病理学及透射电镜检查.对实验数据用t检验的方法进行统计学分析.结果 复苏组在ROSC后各时间点,左心室收缩期压力最大上升速率、左心室舒张期最大下降速率、心排血量与致颤前相比均明显降低,差异具有统计学意义(P＜0.05),复苏组ROSC后各时间点HR较致颤前明显增加(P＜0.05),各时间点MAP之间比较差异无统计学意义(P＞0.05);通过对苏木精-伊红(HE)染色切片及透射电镜切片的观察,进行正常组与复苏组动物各主要脏器组织病理学比较,心搏骤停室颤-心肺复苏模型中猪的心肌、大脑、肺脏、肝脏及肾脏组织均存在不同程度的病理损伤,以心肌、大脑、肺脏的损伤更为严重.结论 心搏骤停-心肺复苏对机体各主要脏器均可以造成不同程度的形态学损伤及血流动力学影响,在ROSC成功6 h的模型中,以心肌、大脑及肺的损伤较重,肝、肾的损伤较轻.     

他汀类药物干预后细胞再移植对梗死心肌的影响

目的 观察在应用阿托伐他汀基础上进行间充质干细胞(MSCs)移植对梗死心肌修复的影响及其治疗急性心肌梗死(AMI)的可行性.方法 体外获取、培养大鼠骨髓MSCs;结扎左冠状动脉前降支,建立AMI模型.存活大鼠随机分为4组:应用阿托伐他汀并行MSCs移植组(A组)、阿托伐他汀组(B组)、MSCs移植组(C组)、AMI对照组(D组).A、B组术后给予阿托伐他汀10 mg/(kg·d)溶水2 ml,灌喂10 d;C、D组正常喂养.10 d后再次开胸,A、c组分别在梗死部位5个点移植MSCs,每点2×106/50μl;B、D组于相同部位注射同剂量磷酸盐缓冲液.3周后,检测左心室射血分数(LVEF)以及左心室收缩压(LVSP)、左心室舒张末期压(LVEDP)、压力变化最大速率(±dp/dtmax)等指标;免疫组化检测细胞和组织学变化.结果 A、C组与B、D组相比,左心室前壁运动增强,LVEF、LVSP、±dp/dtmax均升高(均P＜0.05),LVEDP降低(P＜0.05),A组较C组改变更明显(P＜0.05).A、C组的梗死心肌内可见5-溴脱氧尿嘧啶(BrdU)标记阳性细胞.对心肌肌钙蛋白T(cTnT)、连接蛋白43(Cx-43)呈现阳性表达.结论 应用阿托伐他汀基础上进行MSCs移植对AMI大鼠心功能有明显的改善作用.     

5-氮胞苷诱导的心室成纤维细胞移植对心肌梗死后心功能的影响

目的：探讨5-氮胞苷诱导的心室成纤维细胞（CFs）植入大鼠梗死区组织后心功能的变化。方法： 取远交群（SD）乳鼠提取CFs,行体外培养、扩增,取第3代细胞以5-氮胞苷诱导。另取20只SD大鼠随机分为治疗组和对照组各10只,建立大鼠AMI模型,2周后,治疗组将诱导后的CFs注入梗死区及其周边;对照组则注入等量细胞培养液。分别在移植前及移植4周后行心脏UCG及MPA心功能分析系统检测心功能。结果：与移植前及对照组移植4周后比较,治疗组移植4周后的左心室收缩末期内径和容积、左心室压最低值、左心室舒张末压明显降低,每搏量、左心室短轴缩短率、左心室射血分数、左心室压最高值、左心室压力上升的最大变化速率及其对应的左心室压、左心室压力下降的最大变化速率及其对应的左心室压明显增加（均为P〈0.05～0.01）。结论： 5-氮胞苷诱导的CFs植入大鼠心肌梗死区可以改善左心室收缩及舒张功能。     

核因子-κB在大鼠烧伤后中性粒细胞致心功能损害中的作用

目的 探讨大鼠烧伤早期核因子-κB(NF-κB)活化对中性粒细胞(PMN)在心肌组织中聚集和发生损害作用的影响.方法 将170只Wistar大鼠随机分正常对照组(20只)、烧伤组(90只)、烧伤后吡咯烷二硫代氨基甲酸盐干预组(PDTC组,60只).后两组大鼠均于背部造成35%体表总面积Ⅲ度烧伤后,立即腹腔注射等渗盐水,且PDTC组同时皮下注射PDTC 250 mg/kg.对照组除不烧伤外,其余处理同烧伤组.伤后1、3、6、12、24 h,凝胶电泳迁移率分析法检测心肌组织NF-κB活性;逆转录-聚合酶链式反应(RT-PCR)检测心肌组织白细胞介素8(IL-8)和细胞间黏附分子-1(ICAM-1)mRNA的表达;八导生理记录仪记录左心室最大收缩压(LVSP)、左心室舒张末压(LVEDP)及心室内压最大上升速率(+dp/dtmax)和下降速率(-dp/dtmax);并测定心肌组织髓过氧化物酶(MPO)活性.对照组作相同检测.数据采用SPSS 10.0统计软件行单因素方差分析.结果 烧伤组大鼠心肌组织NF-κB活性伤后迅速增高,伤后1 h达峰值(20.27±3.43)×104积分灰度值(A),明显高于对照组[(2.18±0.38)× 104A,P＜0.01],伤后24 h仍高于对照组(P＜0.01).伤后3、6、12、24 h心肌组织ICAM-1和IL-8mRNA表达、MPO活性均较对正常对照组明显升高(P＜0.01),:LVSP、±dp/dtmax明显低于正常对照组(P＜0.01),而LVEDP高于正常对照组(P＜0.01).与烧伤组比较,PDTC组上述指标指标均有明显的改善(P＜0.01).结论 严重烧伤可活化心肌组织NF-κB,从而上调黏附分子和趋化因子等的合成和释放,导致PMN在心肌组织中聚集,引起心肌功能损害.     

Increasing percent burn is correlated with increasing inflammation in an adult rodent model

Burn injury has been associated with systemic/compartmental inflammatory responses and myocardial dysfunction. We hypothesized that burn size correlates with the extent of cardiac inflammatory response/contractile dysfunction. Adult male Sprague-Dawley rats were divided to receive anesthesia, a 3-degree burn covering 20%, 30%, 40%, or 60% total body surface area (TBSA) plus fluid resuscitation (lactated Ringer, 4 mL/kg per percent burn); sham burn animals were included as controls. There were seven rats in each group. Rats were euthanized Twenty-four h postburn, and TNF-alpha, IL-1beta, and IL-6 were measured in the plasma and in supernatant from isolated cardiac myocytes by enzyme-linked immunosorbent assay. In addition, left ventricular function (Langendorff) was studied in vitro, and troponin levels were measured by enzyme-linked immunosorbent assay. There were progressive, statistically significant increases in plasma and myocyte inflammatory cytokine levels, as well as plasma troponin with increasing burn size. Similarly, left ventricular pressure (in millimeters of mercury) and +/-dP/dtmax (in millimeters of mercury per second) progressively fell with increasing burn size. However, myocardial contractile depression induced by 60% TBSA burn was similar to that produced by 40% TBSA burn. These data suggest that the degree of inflammatory response, cardiac tissue injury, and myocardial contractile depression were correlated directly with the percent TBSA burn. However, unlike inflammation and cardiac tissue damage, myocardial contractile depression reached a plateau, with maximal myocardial contraction and relaxation defects observed at 40% TBSA burn, which were not further aggravated by a larger (60%) burn.